We have long assumed that pulmonary emboli start as clots in the deep veins of the legs (or pelvis), then break off and float into the branches of the pulmonary artery in the lungs. A huge industry has developed around how best to deal with or prevent this problem, including mechanical devices (sequential compression devices), chemical prophylaxis (heparin products), and physical devices (IVC filters).
The really interesting thing is that less than half of patients who are diagnosed with a pulmonary embolism have identifiable clots in their leg veins. In one study, 26 of 200 patients developed DVT and 4 had a PE. However, none of the DVT patients developed an embolism, and none of the embolism patients had a DVT! How can this kind of disparity be explained?
Researchers at the Massachusetts General Hospital retrospectively looked at the correlation between DVT and PE in trauma patients over a 3 year period. DVT was screened for on a weekly basis by duplex venous ultrsonagraphy. PE was diagnoses exclusively using CT scan of the chest, but also included the pelvic and leg veins to look for a source. A total of 247 patients underwent the CT study for PE and were included in the study.
Here are the factoids:
- Forty six patients had PE (39% central, 61% peripheral pulmonary arterial branches) and 18 had DVT (16 seen on the PE CT and 2 found by duplex)
- Of the 46 patients with PE, only 15% had DVT
- All patient groups were similar with respect to injuries, injury severity, sex, anticoagulation and lengths of stay
- Interestingly, 71% of PE patients with DVT had a central PE, but only 33% of patients without DVT had a central PE.
The authors propose 4 possible explanations for their findings:
- The diagnostics tools for detecting DVT are not very good. FALSE: CT evaluation is probably the “gold standard”, since venography has long since been abandoned
- Many clots originate in the upper extremities. FALSE: most centers do not detect many DVTs in the arms
- Leg clots do not break off to throw a PE, they dislodge cleanly and completely. FALSE: cadaver studies have not shown this to be true
- Some clots may form on their own in the pulmonary artery due to endothelial inflammation or other unknown mechanisms. POSSIBLE
An invited critique scrutinizes the study’s use of diagnostics and the lack of hard evidence of clot formation in the lungs.
Bottom line: this is a very intriguing study that questions our assumptions about deep venous thrombosis and pulmonary embolism. More work will be done on this question, and I think the result will be a radical change in our use of anticoagulation and IVC filters over the next 3-5 years.
Reference: Pulmonary embolism and deep venous thrombosis in trauma: are they related? Arch Surg 144(10):928-932, 2009.
In my last post, I described a case where a fresh trauma patient was found to have an incidental finding of small, distal pulmonary embolus (PE) on her initial trauma evaluation. What should you do when you see this? Reflexively anticoagulate for months?
There are only a few papers dealing with this topic. One is from the MGH, which looked at their experience in screening for deep venous thrombosis (DVT) with duplex ultrasound and diagnosing PE with chest CT. They found that quite a few PEs were found that had no associated DVT in the legs or with clot in the pelvic veins. They also noted an interesting distribution: PEs with no DVT tended to be more distally located, and vice versa for those with DVT. This suggested that some PEs may not be emboli at all, but clot that forms spontaneously in the distal lung circulation.
Scripps Hospital in San Diego did some similar work. Only 31 of some 12,000 patients developed PE, and 19 of these had no identifiable DVT as a source. They also noted that these “de novo” PEs tended to be single and peripherally located. PE associated with DVT tended to be multiple and more central. They also noted an association with chest trauma (pulmonary contusion, rib fractures), blood transfusion, and pneumonia.
Bottom line: As usual, the literature is of little help in this relatively recently identified phenomenon. So what’s the trauma professional to do? Here’s my take. If a PE is found incidentally on the initial trauma evaluation, take a good history to see if there are any family members with clotting problems. Failing that, search for DVT using duplex ultrasound. If the PE is central or multiple, or there is a positive history or duplex screen, anticoagulate as you would any other patient with this problem. If not, carry out the usual prophylaxis and screening as laid out in your usual protocol (you have one, don’t you?), but don’t consider it a “real” PE. At least until we know more about this phenomenon.
For a long time, we “knew” that pulmonary emboli were a possible and dreaded complication of deep venous thrombosis (DVT). However, we are beginning to discover that this is not always the case. The group in San Diego decided to see if there really are two different types of PE in trauma, and what that means.
Scripps Mercy Hospital, a level I trauma center, looked at 5 ½ years of their experience with adult trauma patients who were routinely screened for DVT. Any of these patients who developed a PE within 6 weeks of admission were evaluated further.
Here are the factoids:
- Duplex screening from groin to ankle was carried out twice weekly in ICU patients, and once weekly in ward patients
- Surveillance was carried out if the patient would be non-ambulatory for more than 72 hours, or were at moderate or higher risk for DVT using the ACCP guidelines
- Nearly 12,000 patients were evaluated by the trauma service and 2,881 underwent surveillance
- 31 patients (1%) developed a PE
- 12 of these 31 had DVT identified before or immediately after their PE. Clot was below-knee in 9 (!), above-knee in 2, and in the IJ in one.
- 19 patients had PE but no DVT identified (de novo PE, DNPE)
- DNPE tended to be single and peripherally located, and associated with rib fractures, pulmonary contusions, blood transfusions, and pneumonia
- DVT + PE were more often found in multiple lobes or bilaterally
Bottom line: Like most, this is not a perfect study, but it’s a really good one. It is looking more and more likely that some PEs arise de novo, without any associated DVT. These clots are more likely to be linked to some type of inflammatory process, and have a tendency toward causing more of the classic signs and symptoms of PE. There are still lots of questions to be answered, like do you need to anticoagulate the de novo PEs? But for now, no change in practice. Just be aware that these might not be as bad as they seem.
Reference: Pulmonary embolism without deep venous thrombosis: de novo or missed deep venous thrombosis? J Trauma 76(5):1270-1281, 2014.
Deep venous thrombosis is a common concern in trauma care. Most trauma centers have well defined protocols for prophylaxis and surveillance. Ongoing use of pharmacologic thromboprophylaxis (PTP) in patients with traumatic brain injury (TBI), or in patients who need surgical procedures is controversial. We have all experienced some form of “prophylaxis interruptus”, where our orthopedic or neurosurgical colleagues want us to forego or interrupt ongoing administration of heparin products. Does this create new problems?
A trial was conducted at two Denver trauma centers, trying to clarify the optimal administration of PTP in patients with stable TBI. One cohort received PTP, the other did not (either not indicated, short stay, or already on blood thinners). The group receiving PTP was also stratified into those who received it continuously and those who had interruptions in treatment.
They found that the incidence of DVT and PE was similar for patients receiving PTP vs those not receiving it. The two groups were very different, though, because the ones who did not receive it had less severe injuries and were more likely to be ambulating by discharge. The most interesting finding was that being started on PTP and then interrupting it increased the incidence of DVT fourfold.
What is it about prophylaxis interruptus that is so risky? First, there were only 480 patients in this study, so statistical anomalies could be present. Could it be that the conditions (TBI) and operations that cause it to be interrupted greatly increase the risk? Unfortunately this study can’t answer those questions.
The bottom line: DVT and its prophylaxis is still a muddy concept. What we really need to do is to find out if PTP is really necessary in all the patients in whom we are using it. It would also be helpful if we knew how harmful it really is in patients with significant bleeding in their head, or in patients who need to undergo surgery. One alternative, if this paper pans out, is to begin with mechanical prophylaxis until cleared by neurosurgery and all operations are completed. For now, it’s not yet appropriate to change your existing practice and procedures.
Reference: Interrupted pharmocologic prophylaxis increases venous thromboembolism in traumatic brain injury. J Trauma 70(1):19-26, 2011.The term “prophylaxis interruptus” was coined by Tom Esposito in his discussion of this paper.